28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
These findings suggest that (18)F T807 PET could have value as a biomarker that reflects both the progression of AD tauopathy and the emergence of clinical impairment. 3 key findings →
Evidence: low
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In our training set, people with Parkinson's disease, multiple system atrophy, and dementia with Lewy bodies had lower CSF α-synuclein concentrations than patients with Alzheimer's disease and other neurological disorders. 1 key finding →
Design: cross-sectional Evidence: moderate
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In the new AA diagnostic criteria, AD can be defined clinically as encompassing cognitively normal people having a core 1 AD biomarker. 5 key findings →
Evidence: low
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High WMH was a predictor of progression from normal to MCI (adjusted hazard ratio [HR], 3.30; 95% confidence interval [CI], 1.33-8.17; P= .01) but not conversion from MCI to all-cause dementia. 2 key findings →
Design: cohort study Participants: 67 Evidence: moderate
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In this study, females exhibited higher tau compared with age-matched males, particularly in the setting of elevated Aβ. 5 key findings →
Design: cross-sectional Evidence: low
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The results underscore the impact of education on brain structure and function in LA, highlighting the importance of incorporating educational factors into diagnosing, care, and prevention, and emphasizing the need for global diversity in research. 5 key findings →
Participants: 1,412 Evidence: low
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There was strong agreement regarding the definition of the core clinico-radiological syndrome, meaning that the current consensus statement should be regarded as a refinement, development, and extension of previous single-center PCA criteria rather than any wholesale alteration or redescription of the syndrome. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most prevalent cause of dementia 1 . 4 key findings →
Evidence: low
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Total numbers of global DALYs grew 6·1% (95% UI 4·0-8·1), from 2·64 billion (2·46-2·86) in 2010 to 2·80 billion (2·57-3·08) in 2023, but age-standardised DALY rates, which account for population growth and ageing, decreased by 12·6% (11·0-14·1), revealing large long-term health improvements. 5 key findings →
Evidence: low
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Three survey rounds included 49 to 54 participants that agreed on VasCog-2 diagnostic criteria for preclinical, mild, and major dementia levels of vascular cognitive impairment (under the overarching term VCID). 5 key findings →
Participants: 49 Evidence: low
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In this study, researchers assessed the validity and reliability of an automated labeling system developed to subdivide the human cerebral cortex on magnetic resonance images into gyral based regions of interest. 3 key findings →
Evidence: low
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We studied the accumulation of neurofibrillary tangles (NFTs) and senile plaques (SPs) in 10 Alzheimer's disease patients who had been examined during life. 2 key findings →
Evidence: low
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Amyotrophic lateral sclerosis (ALS) is a fatal degenerative motor neuron disorder.
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Global PET amyloid burden was compared with regards to cognitive status, APOE ɛ4 status, sex, age, and estimated years to symptom onset. 2 key findings →
Design: cross-sectional Participants: 216 Evidence: low
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Gene dosage of the apolipoprotein E (APOE) epsilon 4 allele is a major risk factor for familial Alzheimer disease (AD) of late onset (after age 60). 5 key findings →
Evidence: low
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Furthermore, neuroimaging analysis identified 2 additional loci of high interest for further study. 1 key finding →
Design: case-control study Participants: 168 Evidence: moderate
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The influence of this genetic risk may begin in early life and make an individual more susceptible to cognitive impairment in late life. 1 key finding →
Design: cohort study Evidence: moderate
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After the change point, carriers had a statistically significant cognitive decline with a loss of 0.24 (95% CI, -0.26 to -0.22) points per year for the word list recall test and 2.13 (95% CI, -2.29 to -1.96) points per year for total scores. 5 key findings →
Design: cohort study Participants: 493 Evidence: moderate
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Caregiver stress is associated with negative outcomes for both caregivers and care recipients. 5 key findings →
Design: randomized controlled trial Participants: 14 Evidence: high
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Clinicopathological evidence suggests that the pathology of Alzheimer's disease (AD) begins many years before the appearance of cognitive symptoms. 3 key findings →
Design: cross-sectional Evidence: moderate
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Compared with noncarriers, cognitively unimpaired mutation carriers had elevated mean cortical Pittsburgh Compound B distribution volume ratio levels in their late 20s, and 7 of 9 carriers older than 30 years reached the threshold for amyloidosis (distribution volume ratio level > 1.2). 4 key findings →
Design: cross-sectional Participants: 24 Evidence: low
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Resting-state functional connectivity magnetic resonance imaging changes with progressing AD severity are similar between ADAD and LOAD. 2 key findings →
Design: cross-sectional Participants: 79 Evidence: moderate
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To assess the relationship between dementia, neuronal loss, and neuropathological findings in Alzheimer's disease (AD), we counted the number of neurons, senile plaques, and neurofibrillary tangles in a high-order association cortex. 1 key finding →
Participants: 34 Evidence: low
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Loneliness is a perceived state of social and emotional isolation that has been associated with cognitive and functional decline and an increased risk of incident AD dementia. 5 key findings →
Design: cross-sectional Participants: 25 Evidence: low
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Beneficiaries had an average age of 75.3 years and were predominately female (59%) and non-Hispanic whites (93%). 2 key findings →
Participants: 1,002 Evidence: low
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Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 28,580 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,034 records (3.6% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →